Temporal and anatomical distribution of nitric oxide synthase mRNA expression and nitric oxide production during central nervous system inflammation

López-Figueroa, Manuel O.; Day, Heidi E.W.; Lee, Soon; Rivier, Catherine; Akil, Huda; Watson, Stanley J.

doi:10.1016/s0006-8993(99)02241-6

Cited by 49 publications

(24 citation statements)

References 20 publications

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“…When a ter to the level found in young animals (time6S.E., s: old stimulus, evoking appearance of iNOS mRNA and excess untreated, 13006100; old melatonin, 18006250; young nitric oxide (NO) production in rats is removed, NO levels untreated, 19206120). Acetyl L-carnitine raised the test rapidly return to basal levels [25]. It may be that extended time to 1580690 s, an intermediate value, statistically low-level immune responses are difficult to reproduce in indistinguishable from the values for untreated animals of rodents.…”

Section: 5 Measurement Of Locomotor Activity 7 Statistical Analysesmentioning

confidence: 90%

Reversal of biochemical and behavioral parameters of brain aging by melatonin and acetyl l-carnitine

Sharman

Vaziri

et al. 2002

Brain Research

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Section: 5 Measurement Of Locomotor Activity 7 Statistical Analysesmentioning

confidence: 90%

Reversal of biochemical and behavioral parameters of brain aging by melatonin and acetyl l-carnitine

Sharman

Vaziri

et al. 2002

Brain Research

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“…The production of NO in cultured cells was assayed using the fluorescent probe 4,5-diaminofluorescein diacetate (DAF-2͞DA) as described (8). The cells (10 6 per ml) were incubated in 10 M DAF-2͞DA for 25 min before addition of anti-Fas Ab (10 or 100 ng͞ml).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of mitochondrial respiration by endogenous nitric oxide: A critical step in Fas signaling

Beltrán

Quintero

García-Zaragozá

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

124

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We have found that activation of human adult T cell leukemia (Jurkat) cells with anti-Fas Ab leads, in a concentration-dependent manner, to an early burst of production of nitric oxide (NO), which inhibits cell respiration. This results in mitochondrial hyperpolarization, dependent on the hydrolysis of glycolytic ATP by the F1Fo-ATPase acting in reverse mode. During this early phase of activation, there is a transient release of superoxide anion. All these processes can be prevented by an inhibitor of NO synthase. Approximately 2 h after stimulation with anti-Fas Ab, a distinct second phase can be detected. This comprises a concentrationdependent collapse in mitochondrial membrane potential, a second wave of free radical production, and activation of caspase-8 leading to apoptosis. This second phase is abolished by an inhibitor of caspase activation. In contrast, inhibition of NO synthesis leads to an enhancement and acceleration of these latter processes, suggesting that the early NO-dependent phase represents a protective mechanism. The significance of the two phases in relation to cell survival and death remains to be studied.

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“…Aberrant TNF-α/p55TNFαR1 signaling in the CNS can have a potentially major role in CNS pathologies in which oligodendrocyte death and demyelination is a primary pathological feature [77] . Besides their inflammatory actions, cytokines IL-1β and TNF-α may also be involved in the transcriptional activation of the iNOS gene [78,79] . Microglia in the developing brain have also been shown to express the chemokine receptor CCR5 until 2 weeks of age [80,81] .…”

Section: Nature Of Amcmentioning

confidence: 99%

From blood to brain: amoeboid microglial cell, a nascent macrophage and its functions in developing brain

Kaur

Dheen

Ling

2007

Acta Pharmacologica Sinica

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Amoeboid microglial cells (AMC) in the developing brain are active macrophages. The macrophagic nature of these cells has been demonstrated by many methods, such as the localization of various hydrolytic enzymes and the presence of complement type 3 surface receptors in them. More importantly is the direct visualization of these cells engaged in the phagocytosis of degenerating cells at the ultrastructural level. Further evidence of them being active macrophages is the avid internalization of tracers administered by the intravenous or intraperitoneal routes in developing rats. The potential involvement of AMC in immune functions is supported by the induced expression of major histocompatibility complex class I and II antigens on them when challenged by lipopolysaccharide or interferon-γ. Immunosuppressive drugs, such as glucocorticoids and immune function-enhancing drugs like melatonin, affect the expression of surface receptors and antigens and the release of cytokines by AMC. Recent studies in our laboratory have shown the expression of insulin-like growth factors, endothelins, 2',3'-cyclic nucleotide 3'-phosphodiesterase, and N-methyl-D-asparate receptors. This along with the release of chemokines, such as stromal derived factor-1a and monocyte chemoattractant protein-1, suggests multiple functional roles of AMC in early brain development.

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Temporal and anatomical distribution of nitric oxide synthase mRNA expression and nitric oxide production during central nervous system inflammation

Cited by 49 publications

References 20 publications

Reversal of biochemical and behavioral parameters of brain aging by melatonin and acetyl l-carnitine

Reversal of biochemical and behavioral parameters of brain aging by melatonin and acetyl l-carnitine

Inhibition of mitochondrial respiration by endogenous nitric oxide: A critical step in Fas signaling

From blood to brain: amoeboid microglial cell, a nascent macrophage and its functions in developing brain

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